The object of the proposed study will be to devise techniques to detect and define qualitative alterations in the steroid secretion of aldosterone-producing adrenal tissue. We will consider inborn errors of biosynthesis leading to clinical aldosterone deficiency as well as circumstances in which the biological activity of accumulated intermediates determines the clinical picture. In the latter category may be certain hypertensive syndromes in which the secretion of a mineralocorticoid other than aldosterone or 11-deoxycorticosterone is suspected. Efforts will be concentrated in two hypertensive syndromes in which unknown adrenocortical factors of etiologic importance are strongly suspected. One is a childhood syndrome with evidence of severe mineralocorticoid excess in the absence of detectable secretion of known corticosteroids. The abnormality in this disorder appears to be ACTH-dependent. Another syndrome comprises the large group of adults with benign essential hypertension and low plasma renin activity in which others have suggested abnormally high excretion of the 16 beta-hydroxy derivative of dehydroisoandrosterone as a causative factor. The urinary steroid pattern in both disorders will be defined by gas chromatography/mass spectroscopic techniques.